Mutagenic specificity of the base analog 6-N-hydroxylaminopurine in the URA3 gene of the yeast Saccharomyces cerevisiae

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Abstract

The mutational specificity of the base analog 6-N-hydroxylaminopurine (HAP) was studied in the URA3 gene of the yeast Saccharomyces cerevisiae. Twenty-nine independent HAP-induced ura3 mutations were sequenced. GC→AT transitions were found most frequently (21 out of 29) while AT→GC transitions were less abundant (five out of 29). Three GC→TA transversions were also detected. Two interesting features of DNA context were revealed for transition mutations. One third of the transitions occurred at one site within short direct imperfect repeats converting them to perfect repeats. A model involving complementary interaction of imperfect repeats is proposed to explain the origin of these mutations. Nearly all of the rest of the GC→AT as well as the AT→GC transitions were found in the runs of several identical base pairs, predominantly in the middle or at the 3' template nucleotide of (G)n and (A)n runs.

Original languageEnglish (US)
Pages (from-to)417-421
Number of pages5
JournalMutagenesis
Volume8
Issue number5
DOIs
StatePublished - Sep 1 1993

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Yeast
Saccharomyces cerevisiae
Genes
Yeasts
Mutation
Nucleic Acid Repetitive Sequences
Nucleotides
Base Pairing
DNA
6-N-hydroxylaminopurine
Aeromonas hydrophilia lipase-acyltransferase

ASJC Scopus subject areas

  • Genetics
  • Toxicology
  • Genetics(clinical)
  • Health, Toxicology and Mutagenesis

Cite this

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title = "Mutagenic specificity of the base analog 6-N-hydroxylaminopurine in the URA3 gene of the yeast Saccharomyces cerevisiae",
abstract = "The mutational specificity of the base analog 6-N-hydroxylaminopurine (HAP) was studied in the URA3 gene of the yeast Saccharomyces cerevisiae. Twenty-nine independent HAP-induced ura3 mutations were sequenced. GC→AT transitions were found most frequently (21 out of 29) while AT→GC transitions were less abundant (five out of 29). Three GC→TA transversions were also detected. Two interesting features of DNA context were revealed for transition mutations. One third of the transitions occurred at one site within short direct imperfect repeats converting them to perfect repeats. A model involving complementary interaction of imperfect repeats is proposed to explain the origin of these mutations. Nearly all of the rest of the GC→AT as well as the AT→GC transitions were found in the runs of several identical base pairs, predominantly in the middle or at the 3' template nucleotide of (G)n and (A)n runs.",
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N2 - The mutational specificity of the base analog 6-N-hydroxylaminopurine (HAP) was studied in the URA3 gene of the yeast Saccharomyces cerevisiae. Twenty-nine independent HAP-induced ura3 mutations were sequenced. GC→AT transitions were found most frequently (21 out of 29) while AT→GC transitions were less abundant (five out of 29). Three GC→TA transversions were also detected. Two interesting features of DNA context were revealed for transition mutations. One third of the transitions occurred at one site within short direct imperfect repeats converting them to perfect repeats. A model involving complementary interaction of imperfect repeats is proposed to explain the origin of these mutations. Nearly all of the rest of the GC→AT as well as the AT→GC transitions were found in the runs of several identical base pairs, predominantly in the middle or at the 3' template nucleotide of (G)n and (A)n runs.

AB - The mutational specificity of the base analog 6-N-hydroxylaminopurine (HAP) was studied in the URA3 gene of the yeast Saccharomyces cerevisiae. Twenty-nine independent HAP-induced ura3 mutations were sequenced. GC→AT transitions were found most frequently (21 out of 29) while AT→GC transitions were less abundant (five out of 29). Three GC→TA transversions were also detected. Two interesting features of DNA context were revealed for transition mutations. One third of the transitions occurred at one site within short direct imperfect repeats converting them to perfect repeats. A model involving complementary interaction of imperfect repeats is proposed to explain the origin of these mutations. Nearly all of the rest of the GC→AT as well as the AT→GC transitions were found in the runs of several identical base pairs, predominantly in the middle or at the 3' template nucleotide of (G)n and (A)n runs.

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